HELICOBACTER-PYLORI IN ULCEROGENESIS

Patients with peptic ulcer disease have elevated gastric acid secretio n, hyperfunction of G cell, impaired bicarbonate secretion, increased levels of pepsinogen I and the presence of inflammatory mediators as w ell as Helicobacter pylori-induced gastroduodenitis and gastric metapl asia in the duodenum (in duodenal ulcer patients). Non-H. pylori-assoc iated ulcers include those due to non-steroidal anti-inflammatory drug s, Zollinger-Ellison syndrome, and those related to other forms of gas tritis. Evidence of H. pylori in ulcerogenesis includes the higher pre valence of H. pylori in gastritis and peptic ulcer patients plus the i mportant observation that H. pylori eradication results in healing and long-term cure of ulcer disease. The precise mechanism of mucosal inj ury and ulceration is unclear. Bacterial and inflammatory factors are involved as well as host changes in hormones and gastric acid secretio n.